Afrikaans: Die patogenese en patologie van die hemostatiese versteuringe is deur middel van hematologiese,
histochemiese, lig- en transmissie-elektronmikroskopiese metodes in 2 groepe varke besmet of met virulente
heemadsorberende Afrikaanse varkpes virus isolate of 'n virulente nieheemadsorberende virus isolaat bestudeer.
'n Poging is ook aangewend om die hemostatiese versteurings, bloedings en vaskulere veranderinge by die 2
groepe te probeer vergelyk en moontlike verskille te probeer bepaal. 'n Beraamde trombositopenie en
trombosietdisfunksie is gedurende die laaste 2-3 dae voor dood by beide groepe varke waargeneem. Alhoewel
trombositopenie en trombosietdisfunksie by 'n groter getal varke besmet met die heemadsorberende virus isolate
voorgekom het as by die varke gespuit met die nie-heemadsorberende isolaat, het hierdie veranderinge ook
meer dikwels voorgekom by die varke besmet met die nie-heemadsorberende isolaat wat binne 9 dae
(gemiddelde oorlewingsperiode van groep) dood is. Die graad van trombositopenie en trombosietdisfunksie is
dus blykbaar eerder deur die verloop en strafheid van die siekte as die heemadsorberende eienskap van die
bepaalde virus isolaat bepaal. 'n Besmetting van 'n klein persentasie van die trombosiete met die virus kon in
hierdie studie waargeneem word. Die besmetting van slegs 'n klein persentasie van megakariosiete in die
beenmurg kon elektronmikroskopies waargeneem word. Hieruit is afgelei dat die vermeende trombositopenie by
hierdie varke meer waarskynlik die gevolg van periferele trombosietvernietiging as defektiewe trombositopoeiese
was. Betekenisvolle verlengings van die geaktiveerde gedeeltelike tromboplastientyd, trombientyd, verhoogde
fibrien- en fibrinogeendegradasieprodukvlakke sowel as geringe stygings van die protrombientyd het by die varke
besmet met die heemadsorberende virus isolate voorgekom. By varke wat die nie-heemadsorberende virus
ontvang het, was slegs die trombientyd en fibrinogeendegradasieproduk vlakke verhoog. Die verlenging van die
stollingstye is vertolk as merkbare tekorte van die plasma-stollingsfaktore, die teenwoordigheid van
fibrien- en fibrinogeendegradasie produkte of 'n kombinasie hiervan. Verminderde stolselsametrekking en
varierende grade van oplossing en disintegrasie van stolsels na inkubasie by 37 grade Celsius is beskou as
verdere aanduidings van
gedissemineerde intravaskulere stolling of 'n hiperfibrinolitiese toestand. Wydverspreide nekrose (en sitolise) van
makrofages is in die limfoiede weefsel waargeneem en aanvaar as die moontlike oorsaak van
plasminogeenaktiveerder vrystelling deur makrofages met gevolglike hiperfibrinolise. Hialiene, globulere en
granulere trombi en intravaskulere neerslae, wat swak tot sterk positief vir fibrien gekleur het en ooreengestem
het met 'n toestand van gedissemineerde-intravaskulerestolling, was by alle varke sigbaar. Fibrinoiede
veranderinge van bloedvate kon in verskeie organe maar hoofsaaklik in die limfknope, milt, vel en niere
waargeneem word. Endoteelselbesmetting met die virus kon nie aangetoon word nie. Repliserende Afrikaanse
varkpes viruspartikels kon wel in die sitoplasma van makrofages wat intiem geassosieer was met kapillere
endoteelselle gedemonstreer word. Die fibrinoiede veranderinge ontstaan vermoedelik onder die invloed van
chemiese mediators wat vrygestel word deur besmette makrofages en bloedplaatjies of teenwoordig is in plasma
eerder as deur 'n direkte besmetting van endoteelselle deur die virus. In beide groepe was bloedings mees
uitgesproke in die limfoiede weefsels en was hoofsaaklik gelokaliseer om sinusoidale, kapillere en klein venulere
bloedvate waar die wande nekrotiese veranderinge vertoon het. Hierdie waarneming is vertolk as 'n aanduiding
dat die disintegrasie van kleiner bloedvate 'n belangriker oorsaak van bloeding by die akute siekte as
trombositopenie en onstabiele fibrienstolselvorming verteenwoordig. Hierdie studie verteenwoordig ook die
eerste beskrywing van die bloedings en vaskulere patologiese veranderinge by varke besmet met 'n virulente
nie-heemadsorberende Afrikaanse varkpes virus isolaat.
English: The pathogenesis and pathology of the haemostatic defects in 2 groups of pigs infected either with
haemadsorbing isolates or a non-haemadsorbing isolate of virulent African swine fever virus were studied by
haematological, histochemical and light and transmission electron microscopic methods. A comparison was also
made of the differences in the haemostatic defects, haemorrhages and vascular changes in the 2 groups of pigs.
An estimated thrombocytopenia and thrombocyte dysfunction were observed during the last 2-3 days of life in
pigs from both groups. Although these were present in a greater number of pigs infected with the haemadsorbing
virus isolates they, also occurred more frequently in those infected with the non-haemadsorbing virus which lived
for less than 9 days (mean survival period for group). The estimated degree of these changes was therefore
apparently determined more by the acuteness, duration and severity of the disease than by the haemadsorbing
property of the virus, or lack of it. A small percentage of thrombocytes were found to be infected with the virus.
Only a small percentage of megakaryocytes were found to be infected; this suggests a peripheral destruction of
thrombocytes rather than an impaired thrombocytopoiesis. A significant increase of the activated partial
thromboplastin time, thrombin time, and fibrin and fibrinogen degradation product levels as well as a slight
prolongation of the prothrombin time occurred in the pigs infected with the haemadsorbing virus isolates. In pigs
which received the non-haemadsorbing virus only the thrombin time and fibrinogen-degradation-product levels
were increased. The causes of these changes were considered to be due to coagulation factor deficiencies,
disseminated intravascular coagulation and/or fibrinolysis. This supposition was supported by the reduced clot
retraction and clot dissolution and lysis which occurred after blood was incubated at 37°C. Widespread necrosis
of macrophages was observed in lymphoid tissue and it is postulated that this is responsible for plasminogen
activator liberation by macrophages with consequent fibrinolysis. Hyaline, globular and granular thrombi and
intravascular deposits which stained positively for fibrin were convincing indications of intravascular coagulation
in all pigs. Fibrinoid changes of blood vessel walls were observed in most organs, especially lymph nodes,
spleen, skin and kidneys. Infection of endothelial cells with virus could not be demonstrated. Replicating
intracytoplasmic African swine fever virus particles, however, were present in macrophages associated with
endothelial cells in the lungs and renal glomeruli. The fibrinoid changes are possibly the result of the action of
chemical mediators derived from activated macrophages, blood platelets and plasma rather than the direct effect
of the virus on endothelial cells themselves. In both groups of pigs haemorrhages were more pronounced in
lymphoid tissues and were mainly around small vessels whose walls appeared necrotic. This indicates that
vascular injury is a more important cause of haemorrhage in the acute disease than is thrombocytopenia and
defective fibrin clot formation. This study represents the first description of the haemorrhagic and vascular
pathological changes induced in pigs by a virulent non-haemadsorbing African swine fever virus isolate.
